Acquired immunodeficiency syndrome (AIDS) is caused by two types of human immunodeficiency viruses, collectively designated HIV. HIV is the etiologic agent of AIDS. HIV is transmitted by sexual contact, exposure to blood or blood products, and prenatal infection of a fetus or perinatal infection of a newborn. Antibodies against HIV are nearly always detected in AIDS patients and HIV infected asymptomatic individuals and HIV infection is always detected in AIDS patients and seropositive individuals by culture or amplification of viral RNA and/or
Phylogenetic analysis classifies HIV-1 into groups M (major), N (non-M, non-O), and O (outlier). Group M viruses have spread throughout the world to cause the global AIDS pandemic. In contrast, groups N and O are
relatively rare and endemic to west central Africa. However, group O infections have been identified in Europe and the USA. HIV-1 group M is composed of genetic subtypes (A, B, C, D, F, G, H, J, and K) and circulating recombinant forms (CRFs). The geographic distribution and regional predominance of HIV-1 subtypes and CRFs vary. All subtypes and many recombinant strains exist in Africa with CRF02_AG the predominant strain in west and west central Africa, subtypes A, C, and D predominant in east central Africa, and subtype C predominant in southern Africa.
HIV-1 subtype B is the predominant subtype in the USA, Europe, Japan, and Australia. However, a significant percentage of new HIV-1 infections in Europe are caused by non-B subtypes. In Asia, subtype C is found in India, and CRF01_AE (formerly called subtype E) and subtype B are in Thailand and southeast Asia. South America predominantly has subtypes B and F.
Human immunodeficiency virus type 2 (HIV-2) is similar to HIV-1 in its structural morphology, genomic organization, cell tropism, in vitro cytopathogenicity, transmission routes, and ability to cause AIDS.
However, HIV-2 is less pathogenic than HIV-1, and HIV-2 infections have a longer latency period with slower progression to disease, lower viral titers, and lower rates of vertical and horizontal transmission. HIV-2 is endemic to west Africa but HIV-2 infections, at a low frequency compared to HIV-1, have been identified in the USA, Europe, Asia, and other regions of Africa. HIV-2 is classified into genetic subtypes A-G with most infections caused by subtypes A and B.
The key immunogenic protein and antigenic target for serodetection of HIV infection is the viral (HIV) transmembrane protein (TMP). Antibodies against the TMP (anti-TMP) consistently are among the first to appear at seroconversion of HIV infected individuals. The anti-TMP response remains relatively strong throughout the course of the disease, as evidenced by the near universal presence of antibodies against the TMP in asymptomatic and symptomatic stages of HIV infection. TMPs from HIV-1 groups M and O and HIV-2 are represented in ARCHITECT HIV Ag/Ab Combo reagents by five recombinant antigens and two synthetic
peptides derived from native TMP sequences. The rationale for including three pairs of TMPs is derived from the genetic diversity within HIV-1 and between HIV-1 and HIV-2. Serologic studies indicate that although
HIV-1 and HIV-2 share multiple common epitopes in their core antigens, the envelope glycoproteins are much less cross-reactive. Antibodies elicited against the TMP (or portions of the TMP) of a viral strain within
one group or type may react well, poorly, or not at all with the TMP (or portions of the TMP) from a viral strain of a different group or type. An exception may be antibodies elicited against HIV-1 group N. Early after infection with HIV, but prior to seroconversion, HIV antigen(s) may be detected in serum or plasma specimens. The HIV structural protein most often used as the marker of antigenemia is the core protein, p24. The ARCHITECT HIV Ag/Ab Combo uses anti-HIV p24 in the reagents to detect HIV p24 antigen prior to seroconversion, thereby decreasing the seroconversion window and improving early detection of HIV infection.
Manufacturer’s Reagent package insert, Architect HIV Ag/Ab, May 2014, Abbott Laboratories, MAX-Planck-Ring2, 65205 Wiesbaden, Germany.